Received April 27, 2014
Chitosan (partially deacetylated chitin), a component of fungal cell
walls, caused epidermal cell (EC) death in the leaves of pea (Pisum
sativum L.) and tobacco Nicotiana tabacum or Nicotiana
benthamiana detected by destruction of cell nuclei. The
mitochondria-targeted quinone SkQ1 prevented the destruction of EC
nuclei induced by chitosan. Chitosan increased and SkQ1 suppressed the
activity of protein kinases in N. benthamiana and P.
sativum and eliminated the effect of chitosan. Chitosan induced the
generation of reactive oxygen species (ROS) in the guard cells (GC) of
pea plants. Treatment with chitosan or H2O2 did
not cause destruction of GC nuclei; however, it resulted in disruption
of the permeability barrier of the plasma membrane detected by
propidium iodide fluorescence. Treatment with bacterial
lipopolysaccharide but not peptidoglycan caused destruction of pea EC
nuclei, which was prevented by SkQ1. Leaves of tobacco plants
containing the N gene responsible for resistance to tobacco
mosaic virus (TMV) were infiltrated with Agrobacterium
tumefaciens cells. These cells contained a genetic construct with
the gene of the helicase domain of TMV replicase (p50); its
protein product p50 is a target for the N-gene product. As a
result, the hypersensitive response (HR) was initiated. The HR
manifested itself in the death of leaves and was suppressed by SkQ3.
Treatment of tobacco epidermal peels with the A. tumefaciens
cells for the p50 gene expression stimulated the destruction of
EC nuclei, which was inhibited by SkQ1 or SkQ3. The p50-lacking
A. tumefaciens cells did not induce the destruction of EC
nuclei. The protective effect of mitochondria-targeted antioxidants
SkQ1 and SkQ3 demonstrates the involvement of mitochondria and their
ROS in programmed cell death caused by pathogen elicitors.
KEY WORDS: programmed cell death, mitochondria-targeted quinones,
chitosan, lipopolysaccharide, peptidoglycan, tobacco mosaic virus,
guard cells, epidermal cells